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运动训练可改善离体工作大鼠心脏缺血后的代谢反应。

Exercise training improves metabolic response after ischemia in isolated working rat heart.

作者信息

Bowles D K, Starnes J W

机构信息

Department of Kinesiology, University of Texas at Austin 78712.

出版信息

J Appl Physiol (1985). 1994 Apr;76(4):1608-14. doi: 10.1152/jappl.1994.76.4.1608.

Abstract

Hearts from treadmill-trained and sedentary rats were perfused in the working heart mode. Mechanical and metabolite status was evaluated before ischemia, after 25 min of global ischemia, and after 30 min of retrograde reperfusion. After reperfusion, hearts from trained rats were found to have better recovery of contractile function, lower diastolic stiffness, greater efficiency of work, and greater extracellular calcium responsiveness than hearts from sedentary rats. Training had no significant impact on bioenergetic status before or at the end of ischemia. However, after reperfusion, both phosphocreatine and ATP were significantly higher in hearts from trained rats than from sedentary control rats. Mitochondrial function in both subsarcolemmal and intermyofibrillar subpopulations was unaffected by ischemia-reperfusion. 45Ca2+ uptake during reperfusion was significantly higher in hearts from sedentary rats than from exercise-trained rats. No differences were found in free radical production or tolerance due to training. Therefore, hearts from exercise-trained rats demonstrated an increased metabolic tolerance to ischemic-reperfusion damage, which may contribute to the improved postischemic functional recovery.

摘要

将跑步机训练的大鼠和久坐不动的大鼠的心脏以工作心脏模式进行灌注。在缺血前、25分钟全心缺血后以及30分钟逆行再灌注后评估机械和代谢物状态。再灌注后,发现训练大鼠的心脏比久坐不动大鼠的心脏具有更好的收缩功能恢复、更低的舒张硬度、更高的工作效率和更高的细胞外钙反应性。训练对缺血前或缺血末期的生物能量状态没有显著影响。然而,再灌注后,训练大鼠心脏中的磷酸肌酸和三磷酸腺苷均显著高于久坐不动的对照大鼠。肌膜下和肌原纤维间亚群的线粒体功能不受缺血再灌注的影响。再灌注期间,久坐不动大鼠心脏中的45Ca2+摄取显著高于运动训练大鼠的心脏。未发现训练对自由基产生或耐受性有差异。因此,运动训练大鼠的心脏对缺血再灌注损伤表现出更高的代谢耐受性,这可能有助于缺血后功能恢复的改善。

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